3
Views
1
CrossRef citations to date
0
Altmetric
Original Article

(2″-5″)Oligoadenylate Synthetase Activity in Intestinal Mononuclear and Epithelial Cells of Inflammatory Bowel Disease Patients

, , , &
Pages 941-947 | Received 20 May 1987, Accepted 07 Sep 1987, Published online: 08 Jul 2009
 

Abstract

The activity of (2″-5″)oligoadenylate synthetase, an enzyme induced by and mediating the antiviral action of interferon, was measured in extracts of intestinal mononuclear and epithelial cells isolated from patients with Crohn's disease, ulcerative colitis, and a control group. No significant differences were detected among (2″-5″)oligoadenylate synthetase activities of lamina propria mononuclear cells derived from inflammatory bowel disease-involved and histologically normal control mucosa. Similarly, epithelial cells from inflammatory bowel disease and control patients expressed comparable levels of the enzyme, but these were significantly higher (p < 0.01) than those found in autologous mononuclear cells. These results indicate that interferon is locally produced along the human intestinal mucosa under normal and inflammatory conditions. While this study supports the contention that induction of an antiviral state does not play a significant role in the pathogenesis of inflammatory bowel disease, it does not exclude the activation of the interferon system for other immunologic functions.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.